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Cerebral metabolic effects of strict versus conventional glycaemic targets following severe traumatic brain injury.

ABSTRACT: Optimal glycaemic targets for patients with severe traumatic brain injury remain unclear. The primary objective of this microdialysis study was to compare cerebral metabolism with strict versus conventional glycaemic control.We performed a prospective single-centre randomised controlled within-subject crossover study of 20 adult patients admitted to an academic neurointensive care unit with severe traumatic brain injury. Patients underwent randomised, consecutive 24-h periods of strict (4-7 mmol/L; 72-126 mg/dl) and conventional (<10 mmol/L; 180 mg/dl) glycaemic control with microdialysis measurements performed hourly. The first 12 h of each study period was designated as a 'washout' period, with the subsequent 12 h being the period of interest.Cerebral glucose was lower during strict glycaemia than with conventional control (mean 1.05 [95% CI 0.58-1.51] mmol/L versus 1.28 [0.81-1.74] mmol/L; P?=?0.03), as was lactate (3.07 [2.44-3.70] versus 3.56 [2.81-4.30]; P?

SUBMITTER: Plummer MP

PROVIDER: S-EPMC5784688 | biostudies-other | 2018 Jan

REPOSITORIES: biostudies-other

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Cerebral metabolic effects of strict versus conventional glycaemic targets following severe traumatic brain injury.

Plummer Mark P MP Notkina Natalia N Timofeev Ivan I Hutchinson Peter J PJ Finnis Mark E ME Gupta Arun K AK

Critical care (London, England) 20180125 1

<h4>Background</h4>Optimal glycaemic targets for patients with severe traumatic brain injury remain unclear. The primary objective of this microdialysis study was to compare cerebral metabolism with strict versus conventional glycaemic control.<h4>Methods</h4>We performed a prospective single-centre randomised controlled within-subject crossover study of 20 adult patients admitted to an academic neurointensive care unit with severe traumatic brain injury. Patients underwent randomised, consecuti ...[more]

PMID: 29368635

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Project description:BackgroundAcute respiratory distress syndrome (ARDS) is common after traumatic brain injury (TBI) and is associated with worse neurologic outcomes and longer hospitalization. However, the incidence and associated causes of ARDS in isolated TBI have not been well studied.MethodsWe performed a subgroup analysis of 210 consecutive patients with isolated severe TBI enrolled in a prospective observational cohort at a Level 1 trauma center between 2005 and 2014. Subjects required endotracheal intubation and had isolated severe TBI defined by a head Abbreviated Injury Scale (AIS) score of 3 or greater and AIS score lower than 3 in all other categories. ARDS within the first 8 days of admission was rigorously adjudicated using Berlin criteria. Regression analyses were used to test the association between predictors of interest and ARDS.ResultsThe incidence of ARDS in the first 8 days after severe isolated TBI was 30%. Patients who developed ARDS were administered more crystalloids (4.3 L vs. 3.5 L, p = 0.005) and blood products in the first 12 hours of admission. Patients with ARDS had significantly worse clinical outcomes measured at 28 days, including longer median intensive care unit and hospital stays (4 days vs. 13 days, p < 0.001, and 7.5 days vs. 14.5 days, p < 0.001, respectively). In unadjusted logistic regression analyses, the odds of developing ARDS were significantly associated with head AIS score (odds ratio [OR], 1.8; p = 0.018), male sex (OR, 2.9; p = 0.012), and early transfusion of platelets (OR, 2.8; p = 0.003). These associations were similar in a multivariate logistic regression model.ConclusionIn the era of balanced hemostatic resuscitation practices, severity of head injury, male sex, early crystalloids, and early transfusion of platelets are associated with a higher risk of ARDS after severe isolated TBI. Early transfusion of platelets after severe TBI may be a modifiable risk factor for ARDS, and these findings invite further investigation into causal mechanisms driving this observed association.Level of evidencePrognostic/epidemiologic study, level III.

Project description:OBJECTIVES:To examine the impact of early myocardial workload on in-hospital mortality following isolated severe traumatic brain injury. DESIGN:Retrospective cohort study. SETTING:Data from the National Trauma Databank, a multicenter trauma registry operated by the American College of Surgeons, from 2007 to 2014. PATIENTS:Adult patients with isolated severe traumatic brain injury (defined as admission Glasgow Coma Scale < 8 and head Abbreviated Injury Score ? 4). INTERVENTIONS:Admission rate-pressure product, categorized into five levels based on published low, normal, and submaximal human thresholds: less than 5,000; 5,000-9,999; 10,000-14,999; 15,000-19,999; and greater than 20,000. MEASUREMENTS AND MAIN RESULTS:Data from 26,412 patients were analyzed. Most patients had a normal rate-pressure product (43%), 35% had elevated rate-pressure product, and 22% had depressed rate-pressure product at hospital admission. Compared with the normal rate-pressure product group, in-hospital mortality was 22 percentage points higher in the lowest rate-pressure product group (cumulative mortality, 50.2%; 95% CI, 43.6-56.9%) and 11 percentage points higher in the highest rate-pressure product group (cumulative mortality, 39.2%; 95% CI, 37.4-40.9%). The lowest rate-pressure product group was associated with a 50% increased risk of mortality, compared with the normal rate-pressure product group (adjusted relative risk, 1.50; 95% CI, 1.31-1.76%; p < 0.0001), and the highest rate-pressure product group was associated with a 25% increased risk of mortality, compared with the normal rate-pressure product group (adjusted relative risk, 1.25; 95% CI, 1.18-1.92%; p < 0.0001). This relationship was blunted with increasing age. Among patients with normotension, those with depressed and elevated rate-pressure products experienced increased mortality. CONCLUSIONS:Adults with severe traumatic brain injury experience heterogeneous myocardial workload profiles that have a "U-shaped" relationship with mortality, even in the presence of a normal blood pressure. Our findings are novel and suggest that cardiac performance is important following severe traumatic brain injury.

Project description:BackgroundA minority of persons who have traumatic experiences go on to develop post-traumatic stress disorder (PTSD), leading to interest in who is at risk for psychopathology after these experiences. Complicating this effort is the observation that post-traumatic psychopathology is heterogeneous. The goal of this nested case-control study was to identify pre-trauma predictors of severe post-traumatic psychiatric comorbidity, using data from Danish registries.MethodsThe source population for this study was the population of Denmark from 1994 through 2016. Cases had received three or more psychiatric diagnoses (across all ICD-10 categories) within 5 years of a traumatic experience (n = 20 361); controls were sampled from the parent cohort using risk-set sampling (n = 81 444). Analyses were repeated in samples stratified by pre-trauma psychiatric diagnoses. We used machine learning methods (classification and regression trees and random forest) to determine the important predictors of severe post-trauma psychiatric comorbidity from among hundreds of pre-trauma predictor variables spanning demographic and social variables, psychiatric and somatic diagnoses and filled medication prescriptions.ResultsIn the full sample, pre-trauma psychiatric diagnoses (e.g. stress disorders, alcohol-related disorders, personality disorders) were the most important predictors of severe post-trauma psychiatric comorbidity. Among persons with no pre-trauma psychiatric diagnoses, demographic and social variables (e.g. marital status), type of trauma, medications used primarily to treat psychiatric symptomatology, anti-inflammatory medications and gastrointestinal distress were important to prediction. Results among persons with pre-trauma psychiatric diagnoses were consistent with the overall sample.ConclusionsThis study builds on the understanding of pre-trauma factors that predict psychopathology following traumatic experiences, by examining a broad range of predictors of post-trauma psychopathology and comorbidity beyond PTSD.

Project description:OBJECTIVES:Cerebral edema is a key poor prognosticator in traumatic brain injury. There are no biomarkers identifying patients at-risk, or guiding mechanistically-precise therapies. Sulfonylurea receptor-1-transient receptor potential cation channel M4 is upregulated only after brain injury, causing edema in animal studies. We hypothesized that sulfonylurea receptor-1 is measurable in human cerebrospinal fluid after severe traumatic brain injury and is an informative biomarker of edema and outcome. DESIGN:A total of 119 cerebrospinal fluid samples were collected from 28 severe traumatic brain injury patients. Samples were retrieved at 12, 24, 48, 72 hours and before external ventricular drain removal. Fifteen control samples were obtained from patients with normal pressure hydrocephalus. Sulfonylurea receptor- 1 was quantified by enzyme-linked immunosorbent assay. Outcomes included CT edema, intracranial pressure measurements, therapies targeting edema, and 3-month Glasgow Outcome Scale score. MAIN RESULTS:Sulfonylurea receptor-1 was present in all severe traumatic brain injury patients (mean = 3.54 ± 3.39 ng/mL, peak = 7.13 ± 6.09 ng/mL) but undetectable in all controls (p < 0.001). Mean and peak sulfonylurea receptor-1 was higher in patients with CT edema (4.96 ± 1.13 ng/mL vs 2.10 ± 0.34 ng/mL; p = 0.023). There was a temporal delay between peak sulfonylurea receptor-1 and peak intracranial pressure in 91.7% of patients with intracranial hypertension. There was no association between mean/peak sulfonylurea receptor-1 and mean/peak intracranial pressure, proportion of intracranial pressure greater than 20 mm Hg, use of edema-directed therapies, decompressive craniotomy, or 3-month Glasgow Outcome Scale. However, decreasing sulfonylurea receptor-1 trajectories between 48 and 72 hours were significantly associated with improved cerebral edema and clinical outcome. Area under the multivariate model receiver operating characteristic curve was 0.881. CONCLUSIONS:This is the first report quantifying human cerebrospinal fluid sulfonylurea receptor-1. Sulfonylurea receptor-1 was detected in severe traumatic brain injury, absent in controls, correlated with CT-edema and preceded peak intracranial pressure. Sulfonylurea receptor-1 trajectories between 48 and 72 hours were associated with outcome. Because a therapy inhibiting sulfonylurea receptor-1 is available, assessing cerebrospinal fluid sulfonylurea receptor-1 in larger studies is warranted to evaluate our exploratory findings regarding its diagnostic, and monitoring utility, as well as its potential to guide targeted therapies in traumatic brain injury and other diseases involving cerebral edema.

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Cerebral metabolic effects of strict versus conventional glycaemic targets following severe traumatic brain injury.

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Cerebral metabolic effects of strict versus conventional glycaemic targets following severe traumatic brain injury.

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